Long non-coding RNAs involved in autophagy regulation

Yang, Li; Wang, Hanying; Shen, Qi; Feng, Lifeng; Jin, Hongchuan

doi:10.1038/cddis.2017.464

Cited by 125 publications

(92 citation statements)

References 136 publications

(189 reference statements)

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“…Long non-coding RNAs (LncRNAs), a class of non-coding RNA, are characterized by non-coding transcripts longer than 200 nucleotides in length with no open reading frame, which function as decoys, scaffolds, guides, and enhancers to regulate DNA, RNA and proteins. 4 Among the identified lncRNAs, long non-coding RNA maternally expressed gene 3 (lnc-MEG3) is reported to be positively associated with inflammation and organ injury. 5,6 For instance, lnc-MEG3 enhance inflammatory response via upregulating the expressions of early growth response protein 1 and Toll-like receptor 4.…”

Section: Introductionmentioning

confidence: 99%

Lnc‐MEG3 acts as a potential biomarker for predicting increased disease risk, systemic inflammation, disease severity, and poor prognosis of sepsis via interacting with miR‐21

Lei

Ding

Xing

et al. 2020

Clinical Laboratory Analysis

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: This study aimed to investigate the correlations of long non-coding RNA maternally expressed gene 3 (lnc-MEG3), microRNA (miR)-21, and lnc-MEG3/miR-21 axis with disease risk, inflammation, disease severity, and 28-day mortality of sepsis. Methods: Totally, 219 sepsis patients and 219 health controls (HCs) were enrolled. Plasma samples were obtained from sepsis patients within 24 hours after admission and from HCs on enrollment to detect lnc-MEG3 and miR-21 expressions by realtime quantitative polymerase chain reaction. Results: The lnc-MEG3 expression and lnc-MEG3/miR-21 axis were increased, while miR-21 expression was decreased in sepsis patients compared with HCs. Lnc-MEG3 (area under the curve (AUC): 0.887, 95% confidence interval (CI): 0.856-0.917) andlnc-MEG3/miR-21 axis (AUC: 0.934, 95% CI: 0.909-0.958) had good values for predicting elevated sepsis risk, while miR-21 (AUC: 0.801, 95% CI: 0.758-0.844) presented a good predictive value for reduced sepsis risk. Furthermore, lnc-MEG3 expression and lnc-MEG3/miR-21 axis positively correlated with, whereas miR-21 expression negatively correlated with acute pathologic and chronic health evaluation II, sequential organ failure assessment score, serum creatinine, C-reactive protein, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-17 in sepsis patients. Additionally, lnc-MEG3 (AUC: 0.704, 95% CI: 0.626-0.783) and lnc-MEG3/miR-21 axis (AUC: 0.669, 95% CI: 0.589-0.750) exhibited acceptable values in predicting higher 28-day mortality risk, while miR-21 (AUC: 0.588, 95% CI: 0.505-0.672) presented a poor predictive value for lower 28-day mortality risk in sepsis patients. Conclusion:Lnc-MEG3 might serve as a potential biomarker for the development, progression, and prognosis prediction of sepsis via interacting with miR-21.

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Section: Introductionmentioning

confidence: 99%

Lnc‐MEG3 acts as a potential biomarker for predicting increased disease risk, systemic inflammation, disease severity, and poor prognosis of sepsis via interacting with miR‐21

Lei

Ding

Xing

et al. 2020

Clinical Laboratory Analysis

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“…In contrast to PTENP1 , the lncRNA HOTAIRM1 impedes autophagy by inhibiting all‐trans retinoic acid (ATRA)‐induced cell autophagy of PML‐RARA in promyelocytic leukemia (PML) . Interestingly, however, upon binding miR‐20a/106b and miR‐125b for enhancing ULK1, E2F1 and DNA damage regulated autophagy modulator 2 expression, HOTAIRM1 can additionally promote autophagy, contributing to autophagy‐dependent degradation of PML‐RARA . Thus, overexpression of HOTAIRM1 may serve as a potential therapeutic measure for PML.…”

Section: Lncrnas Involved In Cancer Viabilitymentioning

confidence: 99%

“…60,153,154 Interestingly, however, upon binding miR-20a/ 106b and miR-125b for enhancing ULK1, E2F1 and DNA damage regulated autophagy modulator 2 expression, HOTAIRM1 can additionally promote autophagy, contributing to autophagydependent degradation of PML-RARA. 60,155 Thus, overexpression of HOTAIRM1 may serve as a potential therapeutic measure for PML. The lncRNA, maternally expressed gene 3 (MEG3), a wellstudied tumor suppressor, simultaneously affects cell apoptosis and autophagy in multiple cancers.…”

Section: Lncrnas Involved In Cancer Viabilitymentioning

confidence: 99%

Regulatory roles of long noncoding RNAs implicated in cancer hallmarks

Wang

Zhang

Chen

et al. 2019

Intl Journal of Cancer

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Cancer cells acquire numerous biological properties (designated “cancer hallmarks”), such as cell survival and energy metabolism, that facilitate tumor growth and metastatic dissemination during development. To date, eight hallmarks of cancer have been identified that provide a logical framework for understanding the remarkable diversity of neoplastic diseases, as proposed by Douglas Hanahan and Robert A. Weinberg. Long noncoding RNAs (lncRNAs), a category of transcripts widely demonstrated to exert significant regulatory effects on biological processes, have attracted considerable research attention due to their association with the occurrence and development of cancer. The mechanisms by which lncRNAs exert their functions require elucidation to optimize their potential utility as alternative biomarkers and therapeutic targets during tumor occurrence and progression. In this review, we have discussed recent research progress on lncRNAs involved in various cancer hallmarks and their related mechanisms of action, with a view to providing an updated picture of their immense therapeutic potential in the fight against cancer.

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“…When levels of AMP are increased (such as in ischaemic conditions where energy is limited) AMPK is activated by phosphorylation. This inhibits mTORC1, resulting in activation of autophagy, as mTORc1 has an inhibitory effect on autophagy through several regulatory factors (Yang L et al, 2017;Li H et al, 2018;Perez-Alvarez et al, 2018). By inhibition of mTORc1, ULK-1 is activated and beclin-1 complex recruited to catalyse the formation of PI3P.…”

Section: Figurementioning

confidence: 99%

Pharmacological Modulation of Autophagy for Neuroprotection in Ischaemic Stroke

Gunn¹,

Singh²,

Diao³

et al. 2018

J Exp Stroke Transl Med

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Autophagy is a highly regulated, catabolic process, through which macromolecules such as damaged organelles and proteins are degraded and recycled to maintain cellular homeostasis. Various studies have shown the role of autophagy activation in the brain cells such as astrocytes, microglia, neurons and capillary endothelial cells upon an ischaemic insult. The underlying mechanism and the role of autophagy in ischaemic stroke, however, are yet to be fully elucidated. Recent studies have suggested that insufficient or excessive autophagy results in nerve damage and cell death whereas mild/moderate autophagy has a neuroprotective effect. It has been proposed that autophagy may be a therapeutic target in stroke treatment; however, there is a lot of debate as to whether induction or diminution of autophagy plays a role in neuronal survival after cerebral ischaemia and indicate that it has a dual role depending on the time of induction of autophagy. This review has summarized the role of autophagy in ischaemic stroke and explored effects of pharmacological autophagy modulators in ischaemic stroke treatment. Further studies are needed for translating the potential therapeutic approach in stroke treatment aiming at characterizing the timing, amount and specificity of the autophagy modulation.Recently, studies have found autophagy to be a key regulatory factor in ischemic stroke, unveiling a new range of potential therapeutic targets for neuroprotection (Papadakis et al., 2013). Nevertheless, the full mechanism has not yet been construed, hence, there is still controversy over whether autophagy is neuroprotective or pro-death under hypoxia (Wang et al., 2018a). The aim of this review article is to elucidate the role of autophagy in ischaemic stroke and explore pharmacological modulation of autophagy as therapeutic use for neuroprotection in ischaemic stroke.

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Long non-coding RNAs involved in autophagy regulation

Cited by 125 publications

References 136 publications

Lnc‐MEG3 acts as a potential biomarker for predicting increased disease risk, systemic inflammation, disease severity, and poor prognosis of sepsis via interacting with miR‐21

Lnc‐MEG3 acts as a potential biomarker for predicting increased disease risk, systemic inflammation, disease severity, and poor prognosis of sepsis via interacting with miR‐21

Regulatory roles of long noncoding RNAs implicated in cancer hallmarks

Pharmacological Modulation of Autophagy for Neuroprotection in Ischaemic Stroke

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